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Dissertation on
THE ROLE OF FUNDUS FLUORESCEIN ANGIOGRAPHY
AND OPTICAL COHERENCE TOMOGRAPHY IN DIABETIC
MACULOPATHY – A CLINICAL STUDY
Submitted in partial fulfillment of requirements of
M.S. OPHTHALMOLOGY
BRANCH – III
REGIONAL INSTITUTE OF OPHTHALMOLOGY
MADRAS MEDICAL COLLEGE
CHENNAI- 600 003
THE TAMILNADU
DR.M.G.R. MEDICAL UNIVERSITY
CHENNAI
APRIL 2012
2
CERTIFICATE
This is to certify that this dissertation entitled “THE ROLE OF
FUNDUS FLUORESCEIN ANGIOGRAPHY AND OPTICAL
COHERENCE TOMOGRAPHY IN DIABETIC MACULOPATHY – A
CLINICAL STUDY” is a bonafide record of the research work done by
Dr.N.SUGANYA., Post graduate in Regional Institute of Ophthalmology,
Madras Medical College and Research Institute, Government General
Hospital,Chennai-03, in partial fulfillment of the regulations laid down by
The TamilNadu Dr.M.G.R. Medical University for the award of M.S.
Ophthalmology Branch III, under my guidance and supervision during the
academic years 2009-2012.
Prof. Dr. A.SULAIMAN M.S., D.O H.O.D of Retina Services
RIOGOH, Chennai- 600008
Prof. Dr.K.VASANTHA M.S , FRCS Director and Superintendent,
Regional Institute of Ophthalmology
Madras Medical College
Chennai – 600 008
Dr. V. KANAGASABAI, MD, Ph.D Dean,
Madras Medical College &
Govt. General Hospital,
Chennai-600 003
3
REGIONAL INSTITUTE OF OPHTHALMOLOGY
MADRAS MEDICAL COLLEGE
CHENNAI- 600 003
DECLARATION BY THE CANDIDATE
I hereby declare that this dissertation entitled “THE ROLE OF
FUNDUS FLUORESCEIN ANGIOGRAPHY AND OPTICAL
COHERENCE TOMOGRAPHY IN DIABETIC MACULOPATHY – A
CLINICAL STUDY” is a bonafide and genuine research work carried out by
me under the guidance of Prof. Dr. Jayasungathi, M.S.D.O.,
Prof. Dr.Sulaiman, M.S.,D.O., Prof. Dr.Revathi M.S.,D.O., Professors,
Department of Retina Services, Regional Institute of Ophthalmology &
Government Ophthalmic hospital, Chennai – 600008.
Date: Dr.Suganya.N
Place:
4
ACKNOWLEDGEMENT
I express my sincere thanks and gratitude to
Prof. Dr. V. KANAGASABAI M.D., Ph.D., Dean, Madras Medical
College for permitting me to conduct this study..
I have great pleasure in thanking professor
Dr. K. VASANTHA, M.S.,F.R.C.S., Director and Superintendent RIO
– GOH, Madras Medical College, Chennai, for her valuable advice in
preparing this dissertation.
I express my profound gratitude to Prof. Dr. Jayasuganthi M.S.
D.O., Prof. Dr.Sulaiman, M.S.,D.O., Prof. Dr.Revathi M.S.,D.O., my
unit chiefs and for their valuable guidance and constant support at every
stage throughout the period of this study.
I am very grateful to my unit assistants Dr. Rajasekar M.S.,
Dr. Balaji M.S., Dr. Sivagami M.S., for rendering their valuable
advice and guidance for the study.
I wish to express my sincere thanks to all the professors, assistant
professors and all my colleagues who had helped me in bringing out this
study.
Finally, I am indebted to all the patients for their sincere co-
operation for the completion of this study.
5
CONTENTS
S. NO. TITLE PAGE
NO.
PART - I
1 INTRODUCTION 3
2 ANATOMY OF MACULA 4
3 CLINICAL ASSOCIATIONS AND RISK
FACTORS
8
4 PATHOPHYSIOLOGY OF DIABETIC
MACULAR EDEMA
10
5 CLINICAL PRESENTATION 12
6 FUNDUS FLUORESENCE PATTERNS OF
DIABETIC MACULAR EDEMA
18
7 OPTICAL COHERENCE TOMOGRAPHY
PATTERNS OF DIABETIC MACULAR
EDEMA
24
8 MANAGEMENT 30
PART-II
9 AIM OF THE STUDY 39
10 INCLUSION AND EXCLUSION CRITERIA 40
11 MATERIALS AND METHODS 40
12 OBSERVATION AND RESULTS 43
13 DISCUSSION 61
14 CONCLUSION 63
PART – III
15 BIBLIOGRAPHY 69
16 PROFORMA 71
17 MASTER CHART 74
18 KEY TO MASTER CHART 75
6
PART ONEPART ONEPART ONEPART ONE
7
ABBREVIATIONS
DR - Diabetic retinopathy
NPDR - Non proliferative diabetic retinopathy
PDR - Proliferative diabetic retinopathy
FFA - Fundus Fluorescein Angiography
OCT - Optical Coherence Tomography
WESDR - The Wisconsin Epidemiologic Study of Diabetic
Retinopathy
DCCT - The Diabetes Control and Complication Trial
CSME - Clinically significant macular edema
ETDRS - The Early Treatment Diabetic Retinopathy Study
VEGF - Vascular endothelial growth factor
8
INTRODUCTION
Diabetic retinopathy (DR) is a microvascular complication of
both type I and type II diabetes mellitus (DM) has become one of the
leading causes of blindness world wide (Wilkinson 1988)1. It is a
preventable blindness. DR is due to microangiopathy affecting the pre
capillary arterioles, capillaries and venules.
Macular edema is an important and complex component of Non
proliferative diabetic retinopathy (NPDR) and Proliferative diabetic
retinopathy (PDR) and is the major cause of impaired vision. This study
focusses on the role of Fundus Fluorescein Angiography (FFA) and
Optical Coherence Tomography (OCT) in diabetic macular edema and
its management.
9
ANATOMY OF THE MACULA
Anatomically the macula is defined as that portion of the
posterior retina that contains xanthophyllic pigment and two or more
layers of ganglion cells. The macular region is a specialised area of the
central retina with a diameter of 5.5 mm and is centered approximately
4 mm temporal to and 0.8 mm inferior to the centre of the optic disc.
This area can be divided into several regions: the foveola, fovea,
parafoveal area and perifoveal region. The central portion of macula
contains the fovea and the foveola is a small depression in the internal
surface of retina measuring about 0.35 mm in diameter. The fovea is
located about 4mm temporal and 0.8mm inferior to the centre of optic
disc.
The thickness of retina in the fovea is 0.13mm elsewhere it is
0.37 mm.The only photoreceptors in the fovea are cones. The inner
nuclear, inner plexiform,ganglionic cell layer, nerve fibre layers are
absent in the fovea. The entire vascular supply to the fovea is via the
choriocapillaries. The maximal thickness of the retina is at the foveal
margin is 0.55 mm and minimal thickness is at the umbo 0.13 mm.
10
At the macula ganglion cells are more numerous than anywhere
else in the retina. The outer plexiform layer has a reticular structure but
at the macula it is called the Henle ‘s layer. The fibres run at first
vertically, then obliquely near the macula and finally parallel to the
surface. This layer is thickest at the macula and absent at the fovea.
There are no rods in the fovea. 2,3
PARAMETERS OF MACULA
The diameter of fovea - 1.5 mm
The diameter of parafovea - 2.5 mm
The diameter of perifovea - 1.5mm
PARAFOVEA:
It is a central annular zone which contain the largest number of
nerve cells in the entire retina. The thickness of the photoreceptor layer
in this portion of retina is 40 -45 microns.
PERIFOVEA:
The perifoveal retina is situated beyond the parafoveal area .
There are 12 cones per each 100 microns in the perifoveal central
retina.
11
UMBO
It is a tiny depression in the very centre of the foveola which
corresponds to the foveal reflex, loss of which may be an early sign of
damage.
BLOOD RETINAL BARRIER:
The outer blood retinal barrier is formed by the Zona Occludens
between retinal pigment epithelial (RPE) cells.The inner blood retinal
barrier is formed by the tight junctions between retinal capillary
endothelial cells.
VASCULAR SUPPLY
The outer one third of the retina are supplied by the
choriocapillaries. The inner twothird ‘s of the retina are supplied by the
central retinal artery and veins.The inner capillary network is located in
the ganglion cell layer and the outer in the inner nuclear layer. Capillary
free zones are present around arterioles (periarteriolar capillary – free
zone and at the fovea (Foveal avascular zone ).4
Retinal capillaries are devoid of smooth muscle and elastic
tissue and their walls consist of the following:
12
1. Endothelial cells form a single layer on basement membrane and are
linked by tight junctions that form the inner blood retinal barrier.
2. Pericytes lie external to the endothelial cells and have multiple
pseudopodial processes that envelop the capillary. They have
contractile properties and are thought to participate in autoreulation
of microvascular circulation.
HISTOLOGY
Based on light microscopic findings the retina is said to be
composed of ten layers.These from outside to inside are:
1. The pigmented epithelium
2. The rods and cones
3. The external limiting membrane
4. The outer nuclear layer
5. The outer plexiform layer
6. The inner nuclear layer
7. The inner plexiform layer
8. The ganlionic cell layer
9. The nerve fibre layer
10. The internal limiting membrane
13
EPIDEMIOLOGY
The Wisconsin Epidemiologic Study of Diabetic Retinopathy
(WESDR)5
is a study on the progression of diabetic retinopathy.The
duration of diabetes was directly associated with an increased
prevalence of diabetic retinopathy in people with type 1 and type 2
diabetes.After 20 yrs of diabetes, nearly 99% of patients with type 1
and 60% with type 2 had diabetic retinopathy.
It is reported that 3% eyes with mild NPDR, 38% with moderate
to severe NPDR, and 71% eyes with PDR develop Diabetic macular
edema( DME). The incidence increases with advancing retinopathy.
CLINICAL ASSOCIATIONS AND RISK FACTORS
Diabetic macular edema(DME) severity is associated with
1. Diabetic retinopathy severity level
2. Duration of diabetes mellitus : Retinopathy in young patient with
Type I DM does not develop for atleast 3-5 yrs after the onset of the
disease. In type II DM it is difficult to determine the duration for the
development of DR. In patients diagnosed before the age of 30 years,
the incidence of DR after 10 years is 50% and after 30 years it is 90%.
14
DR rarely develops within 5 years of the onset of diabetes or before
puberty, but about 5% of type 2 diabetics have DR at presentation.
3. Glycemic control : The Diabetes Control and Complication
Trial(DCCT)6
hyperglycemia causes breakdown of the blood retinal
barrier by three major mechanisms : increased paracellular permeability
of vascular endothelium, loss of endothelial cell integrity due to cell
destruction, and increased transcellular transport through the
endothelium. Type 1 diabetics appear to obtain greater benefit from tight
control than those with type 2. Raised HbA1c is associated with an
increased risk of proliferative disease.
4. Hypertension : Increased blood pressure increases the risk of
progression of diabetic retinopathy. Tight control appears to be
particularly beneficial in type 2 diabetics with maculopathy.7,8
5. Dyslipedemia
6. Nephropathy : If severe is associated with worsening of DR.
Conversely, treatment of renal disease may be associated with
improvement of retinopathy and a better response to photocoagulation.
7. Fluid retention
15
8. Pregnancy promotes the progression of DR. Predictating factors
include poor pre pregnancy control of diabetes, too rapid control during
the early stages of pregnancy, and the development of pre eclampsia and
fluid imbalance.
9. Intraocular surgery
10. Uveitis
11. Panretinal photocoagulation
12. Anemia induced hypoxia causes the development of
microanuerysms and other retinopathy changes.
13. Genetic factors : There has been found an increased risk of PDR
in subjects with HLA (Human leucocyte antigen) DR4 and DR5
phenotype.
14. Ocular factors : Glaucoma reduced the severity and prevalence of
DR.
PATHOPHYSIOLOGY
There are structural, rheological and biochemical factors that
contribute to the development of DR
16
I. Structural changes
1. Capillary basement membrane thickening
2. Loss of microvascular intramural pericytes
3. Loss of endothelial cells
4. Endothelial cell dysfunction
II. Rheological changes
1. Platelet abnormalities like increased platelet adhesiveness,
increased platelet aggregation, decreased platelet survival.
2. Red blood cell abnormalities like decreased deformability,
increased rouleaux formation.
3. Incresed fibrinogen, alpha 2 macrogobulin and haptaglobulin
III. Biological changes
1. Prolonged hyperglycemia : Several sugars bind non enzymatically
to protein forming advanced glycation end products which are
long lived and play a causal mechanism for the diabetic
complications.
17
2. Sorbitol pathway:
Sorbitol formed from glucose by Aldose reductase is converted
slowly to fructose by sorbitol dehydrogenase.Since the later reaction is
slow sorbitol builds up to toxic concentration leading to endothelial
damage.
3. Increased level of Diacyl glycerol and Protein kinase C which
causes decreased retinal blood flow.
4. Vascular Endothelial Growth Factor is a potent permeability
agent responsible for DME.
CLINICAL PRESENTATION:
Patients with DME present with wide range of visual symptoms
depening on the degree to which fovea is involved. Patients experience
graual progressive vision loss, loss of colour vision, poor night vision,
poor dark light adaptation.
Clinically DME has the following features
a. Thickening of macula
b. Blurring of the underlying choroidal vascular pattern
c. Loss of foveolar light reflex when foveola is involved
d. Cystoid spaces
e. Lipid exudation from the leaking microanuerysms in the form of
ring known as circinate retinopathy.
18
CLASSIFICATION
It is divded into two subtypes Focal and diffuse macular edema.
Focal macular edema
Areas of focal leakage from microanuerysms and dilated
capillary segments characterize focal macular edema. These areas of
focal retinal thickness are delineated from the adjacent healthy retina by
a complete or a partial ring of hard exudates
Diffuse Macular Edema
Diffuse macular edema results from the breakdown of blood
retinal barrier with leakage from microanuerysms and dilated capillary
bed throughout the posterior retina. It has a tendency to be bilaterally
symmetrical. They may disappear spontaneously at the same time in
both eyes even without laser treatment only to reappear later. Systemic
factors like cardiovascular, renal diseases, systemic hypertension, or pre
eclampsia may be associated with exacerbation and amelioration of
diffuse macular edema.
The Early Treatment Diabetic Retinopathy Study(ETDRS)9
criteria for clinically significant macular edema(CSME)
19
1. Thickening of the retina < 500 microns from the centre of the
macula.
2. Hard exudates with thickening of the adjacent retina located 500
microns from the centre of macula
3. A zone of retinal thickening ,1 disc area larger in size located 1
disc diameter from centre of macula.
A simpler classification named International Clinical Diabetic
Macular edema severity scale classified DME as :
Diabetic macular edema absent: No retinal thickening or hard
exudates in the posterior pole.
Diabetic macular edema present: Some retinal thickening or hard
exudates in the posterior pole.
Mild Diabetic macular edema: Retinal thickening or hard exudates in
the posterior pole, but distant from the centre of macula.
Moderate Diabetic macular edema: Retinal thickening or hard
exudates approaching the centre of macula but not involving the centre.
Severe diabetic macular edema: Retinal thickening or hard exudates
involving the centre of macula.
20
Fig.1 FOCAL EDEMA
Fig. 2 DIFFUSE EDEMA
Fig.3 ISCHEMIC EDEMA
21
CLINICAL EVALUATION
1. Visual acuity
Vision loss depends on involvement of the macula.
2. Colour vision
Colour vision is documented by Fransworth Munsell 100 hue test.
The commenest defect is blue yellow.In diabetes the sensitivity of blue
cones are depressed.
3. Fields
Field charting by Tangent screen reveals scotomas corresponding
to the areas of involvement in the fundus.
4. Indirect ophthalmoscopy
This technique allows the entire view of the entire retina.
5. Slit lamp biomicroscopy
6. Direct ophthalmoscopy
This method allows a detailed examination of the fundus with
high magnification.
7. Threshold Amsler grid charting
This is useful in determining the central visual field.
22
8. Photostress test
After images and central scotomas persist after a long time. This
explained the prolonged re-adaptation times in photostress testing the
affected eye.
9. Electrophysiology
i. Electoretinography : Abnormalities of the oscillatory potential in
the ascending limb of b wave and delay in implicit time occurs as
the macular edema progresses.
ii. Electrooculography : Abnormal Arden ‘s ratio will be seen in
DME
iii. Visually evoked potential : The VER shows reduction in
amplitude with no change in latency.
10. Fundus fluorescein angiography
FFA is done for the diagnosis, documentation, identification of
leakage pattern, decision on treatment and the follow up.
11. OCT
This is a valuable tool to diagnose, document, ascertain the
macular thickness, decide about treatment and for the follow up.
23
FUNDUS FLUORESCEIN ANGIOGRAPHY
PRINCIPLES:
FFA is a tool for studying retinal vasculature. In 1910 the two
medical students Harold Novotny & David Alvis produced the first
human FFA. Fluorescein was chemcically related to phenolphthalein &
in alkaline solution forms sodium fluorescein.It is a water soluble,
orange red crystalline hydrocarbon. When injected into the body 80% is
bound to the serum proteins and 20% remains unbound and is referred
to as free fluorescein. Usual dose is 3ml of 20% in adults and 0.04ml/kg
of 20% in children.
The retinal capillary endothelial cells are joined by special
junctional complexes which make them impermeable to fluorescein and
leakage from the retinal circulation is pathological. Major choroidal
vessels are impermeable to both bound and free fluorescein but
choriocapillaries are extremely permeable.
PHASES OF THE ANGIOGRAM:
1. Pre arterial phase or choroidal phase, during which the choroidal
circulation is filling, but no dye has reached the retinal arteries.
24
2. Arterial phase , which follows one second after the pre arterial phase
and extends from the first appearance of the dye in the arteries until
the entire circulation has been filled.
3. Arterio Venous(AV) phase or the capillary phase which is
characterised by complete filling of the arteries and capillaries with
the appearance of early lamellar flow in the veins.
4. Venous phase which is subdivided according to the extent of venous
filling and arterial emptying into early, mid, and late stages.
5. Elimination phase
TECHNIQUE:
Fluorescein, usually 5 ml of a 10% or in eyes with opaque media,
3ml of 25% solution is injected intravenously ino the antecubital vein
over a few seconds images are taken at approximately 1 second
intervals, 5-25 seconds after injection. Late photographs are taken after
10 minutes and occasionly 20 minutes if leakage is anticipated.
PATTERNS OF FLUORESCNCE
1. Hypofluoresence
Vascular filling defects and blocked fluorescence
25
2. Hyperfluorescence
Leakage, staining, pooling, transmission defect.
3. Autofluorescence
It is the appearance of fluorescence without dye injection due to
normally fluorescent structures like drusen and lipofuscin.
4. Pseudofluorescence
It is due to mismatch of the filters in which filter fails to block
unwanted light.
ADVERSE EFFECTS:
Discoloration of skin and urine, nausea, vomiting,, flushing of
the skin, itching, and excessive sneezing. Serious but rare problems
include syncope, laryngeal oedema, bronchospasm and anaphylactic
shock.
DISADVANTAGES
1. Cannot be performed in hazy media
2. Cannot detect lesions under preretinal / subretinal hemorrhage.
26
CONTRAINDICATIONS
History of reaction to the dye
Severe renal or liver dysfunction
FFA CLASSIFICATION OF DME:
Focal Edema:
AV phase shows multiple hyperfluorescent points caused by
microanuerysms bordering the areas of capillary non perfusion. Late
phase shows increased fuzziness around the micoanuerysm due to
leakage of the dye.
Diffuse Edema
Mid AV phase shows leakage of the dye from the dilated
capillaries throughout the macula.It is not associated with hard exudates.
FFA shows early spotty hyperfluorescence of microaneurysm and late
diffuse hyperfluorescence due to leakage, and may be associated with a
flower petal pattern if CME is present. Mostly bilaterally symmetrical.
They may disappear spontaneously at same time in both eyes even
without laser only to reappear spontaneously. The treatment is grid laser
photocoagulation to areas of retinal thickening.
27
Ischemic type:
Retinal capillary nonperfusion is a feature commonly associated
with progressive NPDR. Microanuerysms tend to cluster at the margins
of capillary nonperfusion. Closure of retinal arterioles may result in a
large area of capillary nonperfusion and progressive ischemia.
Clinically the macula is normal. FFA shows enlargement of the foveal
avascular zone greater than 1000µm in diameter. There does not appear
to be a direct correlation between the level of visual acuity and the
severity of ischemia.
It has the following features in FFA
1. Enlargement of Foveal Avascular Zone (FAZ)
2. Irreularities of FAZ
3. Capillary budding into FAZ
4. Widening of intercapillary space and capillary dropout in
perifoveal area.
Treatment is not appropriate in most cases.
Mixed type:
Shows features of both diffuse type of macular edema. and
ischemia.10, 11, 12, 13
28
Fig.4 FOCAL TYPE Fig.5 DIFFUE TYPE
Fig. 6 ISCHEMIC TYPE Fig.7 MIXED TYPE WITH
GRID LASER MARKS
29
OCT
It provides a high resolution, cross sectional images of the macula
and allows the measurement of foveal thickness. It also helped in
determining the vitreo retinal relationship at the macula. OCT is
superior to FFA in detecting cystoid changes. It captures reflected light
from retinal structures to create a cross sectional image of the retina
with an axial resolution of 15 microns.
PRINCIPLE:
It utilises interferometry and low coherence light in the infrared
range (843 nm) to achieve high resolution(about OCT 1 & 2 & about 7
-8 microns for OCT 3), cross sectional imaging of the eye. An optical
beam from a light source which emits short optical pulses or short
coherence length light is directed into two beams, one is reflected and
the other is transmitted.
Advantages to document the clinical efficacy of treatment compared
to conventional FFA:
1. The 2 dimensional cross sectional OCT Scan allows detailed
examination of macular anatomy distinguishing intraretinal,
subretinal and cystoid fluid accumulation
30
2. The false colour image gives topographic image of the central fovea
and perpendicular macular thickness.
3. The measurements are reliable, reproducible and observer
independent.
TECHNIQUE:
Following papillary dilatation 6 radial scans are centered on the
fovea.The retinal architecture is first displayed as a 2 dimensional
image.
The retinal mapping program is employed to process the areas
between 2 neighbouring scans in the periphery & determine the mean
values of all 6 scans in the macula.
OCT SCAN PROTOCOLS IN MACULA :
1. Line scan
2. Radial scan
3. Macular thickness map
4. Fast macular thickness map
5. Raster lines
6. Repeat scan
ANALYSIS PROTOCOL:
1. Retinal thickness
2. Retinal map
3. Retinal thickness/Volume
31
INTERPRETATION:
Pathology categorised either as hyperreflective or hyporeflective
lesion
Hyper reflective lesions
a. Hard exudates
b. Blood
c. Scars
Hypo reflective lesions
In the outermost ring than in the central zone.
a.Serous fluid
b. Hypo pigmented lesions of RPE
The OCT patterns in DME are
1.Sponge like retinal edema:
Thickening of the retina without definite cystic spaces. It is
mostly confined to the outer plexiform and outer nuclear layers due to
back scattering from intra retinal fluid.
2. Cystoid macular edema:
Cystoid cavities are hyporeflective spaces of various sizes mainly
located in the outer retina.In long standing cases they fuse to form large
cyst.
32
3. Serous retinal detachment:
Hypo reflective space under the fovea which may disappear
spontaneously following laser.
4. Tractional macular edema:
Foveo vitreal traction causes detachment of fovea.It is an
indication for Pars Plana Vitrectomy.
5. Taut Posterior Hyaloid Membrane:
It may cause recalcitrant macular edema with foveal detachment. 14, 15
33
Fig.8 SPONGY EDEMA
Fig.9 CYSTOID EDEMA
Fig. 10 SPONGY WITH SEROUS RD
34
Fig.11 VITREOMACULAR TRACTION
Fig.12 TAUT POSTERIOR HYALOID
35
LIMITATIONS AND PIT FALLS:
Retinal thickness in each zone is calculated as the average values
measured on the portion of axis passing through that zone. Therefore
there are fewer points per surface unit in the outermost ring than in the
innermost ring therefore more values are extrapolated.
MANAGEMENT
Treatment strategies for DME encompasses life style modification
exercise, smoking cessation, better control of blood sugar, blood
pressure, blood lipids and body mass index.
PREVENTION AND CONTROL
Diabetes mellitus has multifactorial origin control of the
metabolic abnormalities in diabetes has a major impact on the
development and progression of diabetic microvascular complications.
Diabetes Control and Complication Trial(DCCT) and the united
kingdom prospective diabetes sudy (UKPDS)16
have shown that optimal
metabolic control could reduce the incidence and progression of DR.
Multifactorial control of various risk factors such as HbA1c, blood
pressure, lipid profile, anemia, 24 hrs proteinuria, before laser
photocoagulation led to the reduction in macular edema on OCT. The
36
recommended values for HbA1c,blood pressure, and LDL cholesterol
are <7 percent, <130/80 mmHg, and <100 mg/dl, respectively.
LASER THERAPHY FOR DME:
The goal of macular photocoagulation is to limit vascular leakage
through a series of focal laser burns at leaking microanuerysms or grid
laser burns in regions of diffuse breakdown of the blood retinal barrier.
The ETDRS compared outcomes in eyes assigned to either deferral of
macular laser photocoagulation or immediate treatment for CSME.
The ETDRS used focal laser photocoagulation for the treatment
of DME. Results of the treatment with laser reduced the risk of
moderate visual loss(defined as doubling of the visual angle eg. drop of
3 or more lines in Snellen s equivalent or a drop of 15 or more letters on
ETDRS visual acuity chart ), increased the chance of visual
improvement and was associated with only a minor loss of visual field.17
TREATABLE LESIONS
1. Focal leaks > 500 microns from macular centre causing
thickening or hard exudates.
2. Focal leaks within 300-500 microns from macular centre thought
to be causing thickening or hard exudates.
37
3. Areas of diffuse leakage from microanuerysms and capillary
leakage
4. Avascular zones other than Foveal Avascular Zone ,not treated
previously.
Modified ETDRS Focal/Grid laser photocoagulation of DME
i. Lesions closer than 500µm from the fovea should not be
treated.
ii. Excessive intense and excessive density laser burns should be
avoided
iii. Intraretinal or preretinal hemorrhages should not be treated
iv. Consider treating large (>40µm) microanuerysms that appear to
the principal causes of leakage focally to the ETDRS end point of
colour change(either whitening or darkening).
TECHNIQUE OF FOCAL LASER
Focal refers to direct treatment of all leaking microanuerysms in
the edematous retina between 500-3000 microns from the centre of the
macula with a spot size of 50-100 microns and exposure time of 0.1
second.
38
TECHNIQUE OF GRID LASER
The grid laser is used primarily for areas of diffuse leakage with
no identical focal areas of leakage. It consists of light intensity burns
50 -100 microns in diameter, producing a grid of equally spaced burns,
more than one burn width apart..
LASER TYPES
Most frequently used wavelength are 514nm(the green component
of the Argon Blue/Green laser) &810nm(from the infrared diode laser).
The Argon blue green laser should not be used for the treatment of
microanuerysms that are very close to the central area. This is because
the blue light is absorbed by xanthophylls pigment overlying parafoveal
area, this can cause nerve fibre layer damage and parafoveal scotoma.
SIDE EFFECTS AND COMPLICATIONS
• Paracentral scotoma
• Transient increased edema/decreased vision
• Choroidal neovascularisation
• Sub retinal fibrosis
• Photocoagulation scar expansion
• Inadvertent foveolar burns.18, 19, 20
39
MEDICAL MANAGEMENT OF DME
INTRAVITREAL STEROIDS
The rationale for the use of steroids to treat DME is compelling.
The molecular biology of diabetic vascular change includes
leukostasis, endothelial decompensation and increased levels of
proinflammatory cytokines. Steroids may be useful to treat diabetic
macular edema because of anti-inflammatory effects which include
decreased inflammatory cell activation, adhesion and growth factor
signalling. Steroids have a direct effect on maturation of
interendothelial cell junction and improved barrier properties. The
duration of drug in the vitreous cavity approximates the duration of
clinical effect(2-3 months for 4mg injection of triamcinolone).
In patients with refractory DME intravitreal steroids have been
used. Intravitreal triamcinolone 4mg / 0.1 ml alone or in combination
with laser therapy, has been has been the subject of multiple
investigations of therapy for DME. Patients with a cystoid component to
their ME respond better. Visual decline are often observed 4 – 6 months
after injection. Repeated therapy is often limited by side effects. Side
effects include intraocular pressure elevation, acceleration of cataract,
endophthalmitis, retinal detachment.21
40
INTRAVITREAL ANTI VASCULAR ENDOTHELIAL GROWTH
FACTORS (VEGF)
Angiogenesis formation is central to the pathology of
proliferative diabetic retinopathy and is stimulated by factors such as
VEGF in response to retinal ischemia. VEGF may induce inflammation
by inducing intracellular adhesion molecule –1 (ICAM-1) expression
and leucocyte adhesion. Anti VEGF agents restore the normal
permeability of the blood retinal barrier.
Bevacizumab is a full length, recombinant, humanized,
monoclonal antibody directed against VEGF. In cases of diffuse DME
that failed other treatments, intravitreal injection of bevacizumab
1.25mg in 0.05 ml was associated with improved vision and decreased
retinal thickness 12 weeks after the first injection. However the effect is
transient and the injection needs to be repeated at 4-6 weeks interval.
Pegatinib sodium (Macugen) 0.3 mg/0.05 ml 3 injections at 6
week intervals and were followed for 36 weeks. Pegatinib is a anti
VEGF pegylated aptamer, that specifically binds and neutralises
VEGF165, has been tried in recalcitrant ME.
41
Ranibizumab(Lucentis) is an intravitreally injected,
recombinant, humanized, monoclonal antibody fragment designed to
actively bind and inhibit all isoforms of VEGF.Complications include
endophthalmitis, cataract, vitreous hemorrhage.injection site bleeding
and pain.22
PHARMACOTHERAPY
1. Aldose reductase inhibitors – Sorbinil,Ponalrestat,Tolrestat
Aldose reductase enzyme facilitates the conversion of glucose to
sorbitol.They slow the development of diabetic retinopathy.
2. Advanced Glycation End Products inhibitors
3. Protein kinase inhibitors – Ruboxistaurin Protein kinase C ß is
specifically upregulated in hyperglycemia in tissues like vascular
endothelial cells, and mediates some of the myriad biochemical
disturbances. Ruboxistaurin decreased abnormal vascular
permeability and also inhibited angiogenesis in nondiabetic
retinal ischemia model.
4. Antioxidants : The formation of reactive oxygen species(ROS)
had been known to cause the development of diabetic
complications. Diabetes may cause ROS production through
glucose auto oxidation, increased flux through the polyol
pathway, and increase in protein glycation.
42
Inhibition of superoxide production can effectively block sorbitol
accumulation, AGE formation, and PKC activation.
SURGICAL MANAGEMENT OF DME
Pars plana vitrectomy and detachment of posterior hyaloid is
useful in treating DME when there is evidence of posterior hyaloidal
traction and taut posterior hyaloid. The Diabetic Retinopathy
Vitrectomy Study (DRVS) was established to explore the possibilities
and outcomes of vitrectomy in selected eyes. The results suggest that
early vitrectomy should be considered in eyes with recurrent vitreous
hemmorhage. Additional indications include traction of the disc,
peripapillary retina or macula that distorts these structures and lead to
reduction in vision, opaque fibrous proliferation in front of the retina
and extensive pre retinal hemorrhage.
Vitrectomy with or without membrane peeling of posterior
hyaloid membrane may be beneficial for the treatment of DME in eyes
that are resistant to laser photocoagulation.23
43
PART PART PART PART TTTTWOWOWOWO
44
AIM OF THE STUDY
i. To study the prevalence of diabetic maculopathy in relation to
age, gender, duration of diabetes mellitus.
ii. To classify diabetic maculopathy using FFA & OCT
iii. To treat diabetic maculopathy according to FFA & OCT
classification.
iv. To monitor the response to treatment with OCT.
45
MATERIALS AND METHODS
This study was conducted in Regional Institute of Ophthalmology And
Government Ophthalmic Hospital, Egmore, Chennai from November 2009 to
November 2011 for a period of 24 months.
INCLUSION CRITERIA:
All patients with clinically significant macular edema and with
central subfield macular thickness more than 200 microns.
EXCLUSION CRITERIA:
i. History of severe systemic disease/steroids
ii. Uncontrolled Diabetes mellitus/Hypertension
iii. Any condition affecting follow up.
iv. History of associated glaucoma/ocular hypertension
v. History or evidence of ongoing uveitis
vi. Advanced diabetic eye disease
All the patients were taken a brief history and subjected to detailed systemic
and ophthalmic examination. Anterior segment examination with slit lamp
biomicroscope and posterior segment examination using 90 D, binocular indirect
ophthalmoscope. Fundus photograph was also taken for documentation. Fundus
fluorescein angiography, Optical coherence tomography were done for all patients.
46
Focal Photocoaulation was done for focal leak at peri and parafoveal area
signifying macular edema. Direct treatment of leaking microanuerysms, were
carried out with 50 to 100µ spot size of Nd Yag laser for 0.05 to 0.1 sec to produce
mild to moderate burns.
Grid pattern photocoagulation was done for diffuse leak with 50 to 100µ spot
size for 0.05 to 0.1 sec. Modified grid (Both focal and grid laser) were done for
patients with mixed type of maculopathy. Ischemic maculopathy associated with
ischemia elsewhere in fundus were given scatter photocoagulation and kept under
observation.
Patients with Cystoid macular edema in OCT and refractory diffuse DME
unresponsive to focal/diffuse laser photocoagulation were treated with intravitreal
injection of Triamcinolone acetonide (4 mg/0.1 ml). Pre& post treatment follow up
was done with OCT to find the treatment response. Patients with Vitreomacular
traction (VMT) and Taut posterior hyaloid (TPH) patterns in OCT were planned for
vitrectomy.
INTRAVITREAL injections procedure:
Injection procedure guidelines include consideration of pre existing
conditions such as active external infection, eyelid abnormalities, povidone iodine,
lid scrubs, preinjection topical antibiotics, lid speculum, drape, gloves, topical
anaesthesia and post injection topical antibiotics. The risk of endophthalmitis
following intravitreal injection is estimated to be approximately < 0.1%.
47
Guidelines for intravitreal injection:
Draping the ocular surface, eye lid, and eye lashes with povidone iodine,
usage of lid speculum and avoidance of contamination of the needle with eye lid
margin. Pupil should be dilated, topical anaesthetic drops should be applied before
injection. Intraocular pressure(IOP) should be checked following injection.
FOLLOW UP:
Patients were followed up after 4 th,8 th & 16 th week, following laser
photocoagulation. Following intravitreal injection patients were followed up on the
immediate day following injection. They were followed up every week for 1 month,
then every 2 weeks subsequently upto 6 months.
Main outcome measures:
1 .Best corrected visual acuity before & after treatment(Snellen’s chart)
. 2. Macular thickness by OCT.
3. IOP should be measured by Goldmann ‘s applanation tonometry.
48
0
5
10
15
20
25
30
35
40
21-30 31-40 41-50 51-60 61-70 71-80
OBSERVATION AND ANALYSIS
1. AGE DISTRIBUTION
Table 1
Age group(years) No of patients Percentage
21 - 30 2 4%
31 - 40 6 12%
41 - 50 19 38%
51 - 60 12 24%
61 - 70 9 18%
71 - 80 2 4%
In our study the predominant age group affected is the 41-50 years range 38%
followed by 51-60 years range 24% and 61-70 years range 18%. In our study 60%
of cases are aged between 41-60.This correlates with the Wisconsin Epidemiological
study 5of Diabetic Retinopathy revealed diabetic retinopathy more prevalent in the
middle aged population affecting people aged 41-60 years.
49
2. SEX DISTRIBUTION
Table 2
Sex No. of Cases Percentage
Male 27 54%
Female 23 46%
In our study, males were predominantly affected (54%) which correlated
with the Wisconsin Epidemiological Study Of Diabetic retinopathy which showed
a male to female ratio of 1.5:1.
50
0
5
10
15
20
25
30
35
40
45
<5 yrs
<10 yrs
<20 yrs
3. DURATION OF DM
Table 3
Duration No of patients with
DME
Percentage of DME
<5 yrs 12 24%
5-10 yrs 22 44%
10-20yrs 16 32%
1. In our study though the incidence of DME with duration of <5yrs was 24%
2. The incidence was 44% in patients with duration of 5-10 yrs
3. And the incidence of DME with duration of 10-20 yrs was 32%
51
focal
diffuse
ischemic
mixed
4. FFA TYPES
Table 4
Type No. of Cases Total
Focal 18 25 43
Diffuse 17 12 29
Mixed 7 9 16
Ischemic 8 4 12
In our study 43 patients had focal type , 29 had diffuse, 16 had mixed type of
maculopathy and 12 had ischemic maculopathy.
52
spongy
cystoid
cystoidwith SRDSpongywithSRDVMT
TPH
5. OCT TYPES
Table 5
Type No of cases Total
Spongy type 20 24 44
Cystoid type 9 6 15
Cystoid with serous RD 8 11 19
Spongy with serous RD 10 8 18
Vitreomacular
traction(VMT) 2 1 3
Taut posterior
hyaloid(TPH) 1 0 1
In our study 44 patients had spongy type in OCT, 15 had cystoid type,19 had serous
retinal detachment with cystoid pattern, 18 had serous RD . VMT was seen in 3
patients and TPH in 1 patient. This correlated with the study done by Anush goyal
et al which was presented in AIOC.24
53
6. TREATMENT
Table 6
LASER PHOTOCOAGULATION 48
IVTA 34
Laser photocoagulation was done in 48 patients. IVTA was given to
34 patients. 14 patients with ischemic maculopathy were kept under observation
4 patients with VMT and TPH patterns in OCT were planned for vitrectomy. But
2 patients were lost to follow up and 2 patients were not willing for surgery.
7. RESULTS of treatment in DME
Visual acuity on presentation
Table 7
Visual acuity RE LE Total no of pts
<2/60 3 2 5
4/60-6/60 15 17 32
6/36-6/18 19 21 40
<6/12 13 10 23
40 patients had visusl acuity ranging from6/36-6/18 and 23 patients had
visual acuity between <6/12. 48 patients were treated with laser photocoagulation &
34 were given injection IVTA. 18 patients with ischemic maculopathy were kept
under observation . All patients were followed up over a period of 6 months.
54
8. Pretreatment visual acuity (Before laser & IVTA)
Table 8
Visual acuity RE LE Total no of patients
<2/60 0 1 1
4/60 - 6/60 13 14 27
6/60 - 6/18 16 18 34
<6/12 9 20 20
9. Post treatment visual acuity (After laser & IVTA)
Table 9
Visual acuity RE LE Total no of patients
<2/60 2 0 2
4/60-6/60 10 12 22
6/36-6/18 23 16 21
<6/12 16 21 37
Post treatment only 2 patients had visual acuity less than2/60. 37 patients
had visual acuity less than 6/12. 21 patients had VA ranging
from 6/36-6/18 which correlated with the study by Becker et al.25
55
COMPARISON BETWEEN PRE AND POST TREATMENT VISUAL
ACUITY
0
10
20
30
40
<2/60. 4/60 -6/60 6/36-6/18 <6/12
VA
.
The post treatment visual acuity showed an increase with 37 patients having a VA
of < 6 / 12 compared to 20% in the same range before treatment. Chi square test
showed p value< 0.02 on comparing the pre and post treatment visual acuity which
is significant.
10. Pre treatment IOP
Table 10
IOP (mmHg) No of patients
10-12 7
11-13 15
14-16 10
17-19 2
>20 0
56
11. Post treatment IOP
Table 11
IOP(mmHg) No of patients
10-12 4
11-13 16
14-16 8
17-19 3
>20 3
Most patients maintained their IOP within the normal range with 2-4 mmHg
between the pre and post treatment . But 3 patients had IOP >20 mmHg who were
treated with topical 0.5% Timolol eye drops. Their IOP normalised at the end of 6
months.
29. Effect of laser photocoagulation on visual acuity(VA) after 6 months
Table 12
Visual acuity after 4
months No of patients % of visual loss
Improved 31 64.5
Unchanged 12 25
Worsened 5 10.41
Following laser photocoagulation vision improved in 64.5%worsened,
in 10.% which correlated with the study conducted by E G Danes et al,
R G Petty et ea, E M Kohner et al.26
57
0
10
20
30
40
50
60
70
Improved Unchanged Worsened
13. Effect of IVTA on VA after 6 months
Table 13
VA after 4 months No of patients % of visual loss
Improved 22 64.70
Unchanged 10 29.41
Worsened 2 5.88
Following IVTA vision improved in 64.70%, unchanged in
29%,worsened in 5%. Majority of the patients improved after IVTA
injection which correlated with AmJ Ophthalmol 2005:140(4):695-
702.27
V/A after 6 months of laser photocoagulation
58
0
10
20
30
40
50
60
70
Improved Unchanged Worsened
V/A after 6 months of IVTA
14. PRE TREATMENT MACULAR THICKNESS(Before laser
photocoagulation)
Table 14
Macular
thickness(µm)
RE LE Total no of pts
200-400 15 10 25
400-600 4 8 12
600-800 6 3 9
800-1000 2 0 2
59
0
5
10
15
20
25
30
35
<200 200-400400-600600-800 800-
1000
pretreatment
posttreatment
15. POST TREATMENT MACULAR THICKNESS(Following laser
photocoagulation)
Table 15
Macular
thickness
RE LE Total no of pts
<200 15 20 31
200-400 10 9 10
400-600 4 6 5
600-800 0 2 2
Pre treatment macular thickness was between 200-1000µ. 10patients
had macular thickness between 200-400µ. Following laser treatment
majority of patients had macular thickness less than 200µ which
correlated with the ETDRS study.9
COMPARISON BETWEEN PRE AND POST TREATMENT
MACULAR THICKNESS FOLLOWING LASER
Chi square test showed a p value <0.04% on comparing the pre and
post treatment macular thickness which was significant.
60
16. Macular thickness in OCT pre & post treatment in FOCAL
MACULOPATHY:
Table 16
Treatment Decreased Unchanged Increased
laser 29 2 0
IVTA 11 1 0
17. Macular thickness in OCT pre & post treatment in DIFFUSE
MACULOPATHY:
Table 17
Treatment Decreased Unchanged Increased
Laser 9 0 1
IVTA 14 1 1
18. Macular thickness in OCT pre & post treatment in MIXED
MACULOPATHY:
Table 18
Decreased Unchanged Increased
laser 2 1 0
IVTA 11 0 0
61
19. Macular thickness in OCT pre & post treatment in
ISCHEMIC MACULOPATHY:
Table 19
Treatment Decreased Unchanged Increased
observation 3 1 8
Macular thickness in OCT pre & post treatment in focal, diffuse
and mixed maculopathy
0
5
10
15
20
25
focal mixed
decreased
unchanged
incresed
Majority of the cases showed a decresease in macular thickness after
treatment which was documented in OCT.
62
20. Macular thickness in OCT pre & post treatment in SPONGY
EDEMA
TABLE 20
Treatment Decreased Unchanged Increased
laser 33 3 8
21. Macular thickness in OCT pre & post treatment in CYSTOID
EDEMA
Table 21
Treatment Decreased Unchanged Increased
IVTA 14 1 0
22. Macular thickness in OCT pre & post treatment in CYSTOID
EDEMA with SEROUS RD
Table 22
Treatment Decreased Unchanged Increased
IVTA 18 0 1
23. Macular thickness in OCT pre & post treatment in SPONGY
EDEMA with SEROUS RD
Table 23
Treatment Decreased Unchanged Increased
laser 15 1 2
63
24. Macular thickness in OCT pre & post treatment in VMT
Table 24
Treatment Decreased Unchanged Increased
Observation(not willing for
surgery) 0 0 2
Macular thickness in OCT pre & post treatment
0
5
10
15
20
25
30
35
spongy cystoid cystoid/srd spongy/srd
decreased
unchanged
increased
Majority of the cases showed a decrease in macular thickness after
treatment with laser / Inj IVTA.
64
25. Pre treatment macular thickness before IVTA
Table 25
Macular thickness RE LE Total no
200-400 µ 6 4 10
400-600µ 10 5 15
600-800µ 4 3 7
800-1000µ 2 0 2
26. Post treatment macular thickness after IVTA
Table 26
Macular thickness RE LE Total no
<200µ 9 11 20
200 - 400µ 7 4 11
400 - 600µ 2 0 2
600-800µ 0 1 1
The pre treatment macular thickness was between 200 to 1000µ. 10 patients had
macular thickness between 200-400µ. 24 patients had macular thickness between
400 to1000µ. Post treatment all patients had macular thickness less than 600µ
except one patient. 20 patients had reduced thickness <200µ which correlated with
the study published in Br J Ophthalmol 2004, 88(9):1131-6.28
65
Comparison between pre and post treatment macular thickness after IVTA
0
5
10
15
20
<200 200 -
400
400-600 600-800 800-
1000
preIVTA
Chi square test showed a p value,0.02 on comparing the pre and post reatment
macular thickness after IVTA which was significant.
66
CASE 1
Fig. 13 OCT of the LE line scan showing spongy type of macular edema.
Central macular thickness was 480µ
Fig 14. OCT LE after 24 weeks after laser treatment showing a reduction in
the macular thickness to275µ
67
CASE 2
Fig 15. OCT RE line scan showed spongy edema with serous RD with central
macular thickmess of 275µ
Fig. 16 OCT RE showed resolution of the serous RD with central macular
thickness of 208µ after laser treatment
68
CASE 3
Fig. 17 OCT RE line scan showed cystoid type of macular edema with central
macular thickness of 603µ
Fig 18 OCT RE line scan shows reduction in th ecystoid spaces with central
macular thickness reduced to 260µ after injection IVTA
69
DISCUSSION
Diabetic macular edema is the major cause of visual morbidity in diabetic
patients. The laser treatment given by ETDRS remains the standard therapy of
DME. Focal and diffuse types of leaks diagnosed on FFA were treated with focal
and grid laser. Cystoid type and recalcitrant type of macular edema not responding
to laser treatment were given injection IVTA.
1 In our study 27 patients were below 50 yrs and 23 patients were above 50
years. This correlates with the Wisconsin Epidemiological study5
of Diabetic
Retinopathy and revealed diabetic retinopathy more prevalent in the middle
aged population affecting people aged 41-60 years.
2. Males were predominantly affected around 54% which correlated with the
Wisconsin Epidemiological Study5
which showed a male to female ratio of
1.5:1.
3. 24% of patients had DME with 5 years duration, 44% with duration of 5-10
years, & 32% with duration of 10-20 years.
4. In FFA, 43 patients had focal type, 29 patients had diffuse type, 12 had
ischemic type and 16 patients had mixed type of maculopathy.
5. In OCT classification 44 patients had spongy type, 15 patients had cystoid
type, 19 patients had cystoid with serous RD, 18 patients had spongy with
serous RD, 3 patients had VMT and 1 had TPH. This correlated with the
study done by Anush goyal et al which was presented in AIOC24
70
6. 48 pts were treated with laser photocoagulation and 34 pts were treated with
IVTA.
7. Only 2 patients had visual acuity < 2/60 and 37 patients had visual acuity
< 6/12. which correlated with the study by Becker et al.25
Chi square test
showed p value < 0.02 on comparing the pre and post treatment visual
acuity which is significant.
8. After laser treatment 10 patients had macular thickness between 200- 400 µ
and majority had macular thickness <200µ which correlated with the ETDRS
study.9
Chi square test showed a p value < 0.04% on comparing the pre
and post treatment macular thickness which was significant.
9. Following IVTA 20 patients had macular thickness less than 200µ and all
patients had macular thickness less than 600µ which correlated with the
study published in Br J Ophthalmol 2004, 88(9):1131-6.28
Chi square test showed a p value, 0.02 on comparing the pre and post
treatment macular thickness after IVTA which was significant.
10. Following laser photocoagulation VA improved in 64%, worsened in 25%,
unchanged in 10 %. which correlated with the study conducted by E.G
Danes et al, R G Petty et ea, E M Kohner et al.26
11. Following IVTA , VA improved in 64%, unchaned in 29%, worsened in
5%. which correlated with AmJ Ophthalmol 2005:140(4):695-702.27
12. Patients with ischemic maculopathy in FFA and VMT & TPH in OCT had
the worst visual prognosis and their macular thickness was increased over
the period of study.
71
CONCLUSION
In our hospital 100 eyes of 50 patients were studied during NOVEMBER
2009 to NOVEMBER 2011. The incidence of diabetic maculopathy is found to be
commoner in the middle age group of 40-60 years the majority were males and the
incidence of diabetic maculopathy increased with the increase in duration of
diabetes.
Among the FFA patterns focal leaks were commoner and in OCT spongy
edema were the common types. Patients who had ischemic type of maculopathy
were kept under observation and had the worst prognosis over time. The majority of
focal leaks improved with focal laser, and diffuse leaks with grid laser. And
majority of recalcitrant types of macular edema and cystoid type showed
improvement with IVTA injection. Patients with ischemic maculopathy in FFA and
VMT & TPH in OCT had the worst visual prognosis
The overall improvement in visual acuity and the reduction in the macular
thickness was detected and documented by OCT. FFA helped in detecting the
specific leakage patterns and to decide the type of laser treatment. OCT aids in
detecting subtle macular edema that may be difficult to detect on slit lamp
biomicroscopy and in documenting the treatment response. and monitoring the
response to treatment more accurately and less invasively than FFA. OCT & FFA
play a major and complementary role in the diabetic maculopathy management and
follow up.
72
PART THREE
73
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5. Wisconsin epidemiological study of diabetic retinopathy Arch
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6. DCCT Research Group. The relationship of glycemic response
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9. Early Treatment Of Diabetc Retinopathy study Research Group.
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10. Fluorescein photograph of eye textbook by Emanuel S Rosen,
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11. Atlas of FFA by Barbaric A Henry, J Christopic, Rodney H B
Gray
12. Manual of FFA Amrah Choper
13. Colour and fluorescein angiographic atlas of retinal vascular
diseases David orthmd
14. Spectral domain OCT A practical guide Sharun Dacoster Babu
Rajendran P Janakiraman; 73-86.
15. OCT Saxenameredith; 45 - 83.
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progress and performance. Diabetologia.1991;98;823-833.
17. Albert Jakobiec Principles and practice of ophthalmology 1793-
1893
18. OLK RJ Modified Grid laser for diffuse diabetic maculopathy –
ophthal 93:938-958, 1986.
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19. Romanint W, et al. A grid pattern of photocoagulation in the
treatment of diabetic maculopathy. Klinik OC 2&9
102(3):183.06.2000.
20. Kohner EM, Dollery CT, Bulpitt CJ. Cotton wool spots in
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21. Wilon CA, Berkowitz BA, ato Y ando N, Handa JT, de Juan E Jr.
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1992;110:1155-9.
22. Nguyen QD, Tatlipinar S, Shah SM, et al. Vascular endothelial
growth factor is a critical stimulus for diabetic macular
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24. Anush goyal et al AIOC 2010
25. Becker et al survey of ophthalmol jul;64(4):149-152
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28. Bt J Ophthalmol 2004, 88(9):1131-6
76
PROFORMA
Serial No
Name
Age
Sex
OP No.
Occupation
History
a. Complaints (RE/LE)
i. Defective vision
ii. Pain in the eye
iii. Field defects
Past history:
i. Diabetes
Type
Duration
On oral hypoglycemics/inj insulin
ii. Hypertension
Duration
Medication
77
Family history
Systemic examination:
Pulse rate
Blood pressure
RBS
Urine alb & sugar
Ocular examination:
RE LE
Visual acuity -
Conjunctiva -
Cornea -
Anterior chamber -
Iris -
Pupils -
Lens -
Tension(applanation tonometer) -
Fields by Tangent screen -
Colour vision(Ishihara ‘s chart) -
Fundus examination -
By Direct Ophthalmoscopy
By Indirect Ophthalmoscopy
78
Fundus fluorescein angiography : Type of leak
Optical coherence tomography : Macular thickness
Tretment:
Laser photocoagulation:
Type (Focal/Diffuse/Modified Grid)
Power
Spot size
Number of burns
Injection IVTA:
Date
Follow up:
Visual acuity
Macular thickness
79
80
KEY TO MASTER CHRART
VA - Visual acuity
NPDR - Non proliferative diabetic retinopathy
CSME - Clinically significant macular edema
FFA - Fundus fluorescein angiography
OCT - Optical coherence tomography
RE - Right eye
LE - Left eye
IVTA - Intravitreal Triamcinolone acetonide
VMT - Vitreomacular traction
TPH - Taut posterior hyaloid
CME - Cystoid macular edema
